MOSCOW, October 9 – Novosti, Vladislav Strekopytov. For decades, doctors have been trying to understand the nature of Alzheimer’s disease. Traditionally, it, like other types of dementia, is classified as a neurodegenerative disease. However, scientists from Canada have proposed a fundamentally different view – they believe that this is an autoimmune disease and should be treated accordingly.
Acquired Madness
In 1901, the German psychiatrist Alois Alzheimer described the symptoms of senile dementia: problems with memory, speech, orientation in space, mood swings, psychosis, communication difficulties.
As the disease progresses, brain damage becomes more noticeable. The death of nerve cells and the rupture of synaptic connections lead to atrophy of the affected areas and the extinction of neuronal activity in them, the expansion of voids between the lobes of the brain and a decrease in its total volume. Unfortunately, at an early stage, these changes are difficult to notice, and the extent of the lesion can only be assessed after the death of the patient and opening of the skull.
Today, more than 65 million people in the world suffer from dementia. More than ten million new cases are registered annually, two-thirds of which are Alzheimer’s disease. At the same time, experts believe that only 25-30 percent of patients are diagnosed.
Possible reasons
Although dementia consistently ranks second to cancer in terms of publications in scientific medical journals, there is much that is unclear about Alzheimer’s disease. And there are no drugs. Modern therapeutic methods only alleviate the symptoms.
Most scientists adhere to the amyloid hypothesis, linking degeneration processes in the brain with amyloid plaques – deposits of the beta-amyloid protein. However, no significant correlation was found between plaque accumulation and neuronal loss.
There is also the tau hypothesis, which suggests that with certain structural disorders, the tau protein strands combine into neurofibrillary tangles inside nerve cells and neural connections in the brain are broken.
But neurodegenerative changes sometimes appear only years after the formation of plaques and tangles. And what exactly triggers the accumulation of harmful proteins is unknown. Perhaps a bacterial infection is the trigger. The hereditary factor is also not excluded.
Periodically, new, sometimes quite exotic hypotheses are expressed. So, Portuguese scientists recently stated that Alzheimer’s disease is associated with changes in mitochondria – tiny cellular structures responsible for converting glucose from food and oxygen from the air we breathe into energy. Over time, this energy becomes insufficient for the normal functioning of the brain.
Excessive accumulation of iron in the brain, which, when combined with reactive oxygen species, accelerates inflammatory changes and neurodegeneration, is also cited as a possible cause . But of particular interest was the hypothesis formulated recently by Canadian scientists.
Unhealthy Immunity
Biologists at the Krembil Research Institute in Toronto , led by Professor Donald Weaver, based on the results of 30 years of research, have developed a theory according to which beta-amyloid is an immunopeptide, and Alzheimer’s disease is autoimmune.
The immune system is a set of special cells and molecules present in all human organs. In the event of injury or infection, immune agents help repair damaged tissues and build defenses against foreign invaders.
Canadian biologists claim that beta-amyloid is not a harmful newly formed protein, as previously thought, but a natural element of the immune system. In brain injuries or infections, it is a key factor in the complex immune response. And here the problems begin.
Because of the striking similarities between the fat molecules that make up both bacterial and brain cell membranes, beta-amyloid mistakenly attacks healthy cells. This results in a progressive loss of neuronal function and eventually dementia.
Autoimmune diseases (such as rheumatoid arthritis or systemic lupus erythematosus) are chronic, and therapy only alleviates symptoms. With such diagnoses, immunosuppressants, steroid and anti-inflammatory drugs are used.
These methods, according to the authors of the new theory, are unlikely to help with Alzheimer’s disease. The brain is a complex, distinctive organ, separated from the rest of the body by the blood-brain barrier, and the usual drug therapy is not suitable here. However, if the proposed hypothesis is correct, it is theoretically possible to eventually find a treatment based on immune regulation.
